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This study used liver microsomes from control and β-naphthoflavone-treated rats to evaluate NADPH-dependent oxidation of benzidine. With microsomes from β-naphtho-flavone-treated rats, the rates of formation of aqueous soluble metabolite (HPLC analysis) and protein and DNA binding were 835 ±81, 14.5 ± 1.8 and 0.71 ± 0.14 pmol/ mg/min respectively. β-Naphthoflavone treatment elicited 12.3-, 1.8- and 14.2-fold increases in benzidine metabolism compared with controls as judged by HPLC and protein and DNA binding respectively. For microsomes from treated animals,  K  m  and  V  max  values were 47 ± 6 μM and 1.13 ± 0.16 nmol/mg protein/min respectively. All of the metabolic parameters were inhibited to varying degrees by gluta-thione (1 or 10 mM),  N -acetylmethionine (10 mM) and ascorbic acid (10 mM). Following glutathione addition, at least two new metabolite peaks were observed, representing ∼6% of the total radioactivity recovered by HPLC. Neither metabolite was 3-(glutathion- S -yl)benzidine. Cytochrome P450 inhibitors (10 μM) specific for different members of cytochrome gene families 1–3 indicated that benzidine was metabolized by cytochrome P450 1A1/1A2. Ellipticine and α-naphthoflavone, specific 1A1/1A2 inhibitors, elicited 50% inhibition at ∼0.2 and 0.5 μM respectively. Electron impact and negative ion chemical ionization mass spectro-metry identified the aqueous soluble metabolite as 3-hydroxybenzidine. The lability of 3-hydroxybenzidine observed at pH &gt; 7.0 was prevented by ascorbic acid. Thus, cytochrome P450 1A1/1A2 NADPH-dependent metabolism of benzidine to 3-hydroxybenzidine was demonstrated.

NADPH-dependent oxidation of benzidine by rat liver